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1 From the Istituto di Neurofisiologia, Consiglio Nazionale delle Ricerche, Pisa; 2 Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie, Universitá di Pisa; 3 Dipartimento STB, Universitá di L’Aquila, Italy; and the 4 New South Wales Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
Abstract
PURPOSE. To assess the impact of basic fibroblast growth factor (bFGF) on photoreceptor function and morphology.
METHODS. Impact was assessed in two models. In one, the endogenous expression of bFGF in photoreceptors was raised by sectioning one optic nerve of rats 3 to 4 weeks before study. In the other, bFGF was injected into the vitreous chamber in rats and cats. Retinal function was assessed from the electroretinogram (ERG), and retinal morphology was studied using DNA dyes, immunolabeling, and in situ hybridization.
RESULTS. In both models of bFGF upregulation, the ERG b-wave was suppressed over a wide stimulus range and in light- and dark-adapted conditions. The a-wave was not suppressed by either procedure and at the brightest intensities was enhanced by both procedures. In nerve-sectioned eyes, outer retina appeared normal histologically, but levels of bFGF protein in the inner and outer nuclear layers were raised, whereas bFGF mRNA levels remained unchanged. In both models, levels of synaptophysin in the outer plexiform layer and of cytochrome oxidase in inner segments were raised in association with increases in bFGF protein levels.
CONCLUSIONS. bFGF increased the ability of photoreceptors to respond to light but attenuated the transmission of this response to inner retinal cells, presumably by blocking the photoreceptor–bipolar synapse. If the expression of bFGF protein is upregulated in human photoreceptor dystrophies, it may contribute a reversible component to the loss of vision. The relationship between these actions of bFGF and its ability to protect photoreceptors from stress remains to be established.
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